The mechanism of action of IgG-based 4-1BB-agonistic antibodies has been interpreted as a consequence of enhanced antitumor CD8+ T cell responses47, and as the percentage of infiltrating CD8+ T cells is similar in 3H3 IgG- and 1D8N/CEGa1-treated mice, it is likely that both IgG-based anti-4-1BB antibodies and tumor-targeted 4-1BB agonist trimerbody act in a mechanistically equivalent manner. The gene discussed is TNFRSF9; the disease is neoplasm.